Brevetti G, Chiariello M, Ferulano G, et al
[4] A more potent, binding-protein-resistant analog such as IGF-1 LR3 would, by mechanism, be expected to retain this hypoglycemic potential, and because it evades the buffering system that normally tempers free IGF-1 activity, the metabolic effect could in principle be less predictable
The methods range from dietary or intravenous administration of NAD + and precursors to inhibition of NAD + -consuming enzymes with small molecules, to activation of the NAD + synthesis enzymes
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